{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Patton JB"],"funding":["HHS | National Institutes of Health","Howard Hughes Medical Institute","NIDDK NIH HHS","NIAID NIH HHS"],"pagination":["204-209"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5776800"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["115(1)"],"pubmed_abstract":["<i>Strongyloides stercoralis</i> hyperinfection causes high mortality rates in humans, and, while hyperinfection can be induced by immunosuppressive glucocorticoids, the pathogenesis remains unknown. Since immunocompetent mice are resistant to infection with <i>S. stercoralis</i>, we hypothesized that NSG mice, which have a reduced innate immune response and lack adaptive immunity, would be susceptible to the infection and develop hyperinfection. Interestingly, despite the presence of large numbers of adult and first-stage larvae in <i>S. stercoralis</i>-infected NSG mice, no hyperinfection was observed even when the mice were treated with a monoclonal antibody to eliminate residual granulocyte activity. NSG mice were then infected with third-stage larvae and treated for 6 wk with methylpr"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Methylprednisolone acetate induces, and Δ7-dafachronic acid suppresses, <i>Strongyloides stercoralis</i> hyperinfection in NSG mice."],"pmcid":["PMC5776800"],"funding_grant_id":["R01 AI050668","N/A","DK067158","R01 DK067158","AI105856","R21 AI105856","OD P40-10939","R33 AI105856","R01 AI022662"],"pubmed_authors":["Patton JB","Bonne-Annee S","Eberhard ML","Deckman J","Mangelsdorf DJ","Lok JB","Kliewer SA","Abraham D","Torigian A","Durham AC","Hess JA","Lee JJ","Nolan TJ","Wang Z"],"additional_accession":[]},"is_claimable":false,"name":"Methylprednisolone acetate induces, and Δ7-dafachronic acid suppresses, <i>Strongyloides stercoralis</i> hyperinfection in NSG mice.","description":"<i>Strongyloides stercoralis</i> hyperinfection causes high mortality rates in humans, and, while hyperinfection can be induced by immunosuppressive glucocorticoids, the pathogenesis remains unknown. Since immunocompetent mice are resistant to infection with <i>S. stercoralis</i>, we hypothesized that NSG mice, which have a reduced innate immune response and lack adaptive immunity, would be susceptible to the infection and develop hyperinfection. Interestingly, despite the presence of large numbers of adult and first-stage larvae in <i>S. stercoralis</i>-infected NSG mice, no hyperinfection was observed even when the mice were treated with a monoclonal antibody to eliminate residual granulocyte activity. NSG mice were then infected with third-stage larvae and treated for 6 wk with methylpr","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Jan","modification":"2026-05-06T00:27:04.232Z","creation":"2019-03-26T23:44:09Z"},"accession":"S-EPMC5776800","cross_references":{"pubmed":["29203662"],"doi":["10.1073/pnas.1712235114"]}}